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作 者:段志豪 周游 李世刚[4] 金璨 邓颖 柳金浪 马帅[1,2,3] DUAN Zhihao;ZHOU You;LI Shigang;JIN Can;DENG Ying;LIU Jinlang;MA Shuai(Dept.of Orthopedics,the Affiliated Renhe Hospital of China Three Gorges University,Hubei Yichang 443001,China;Sports Medicine Research Institute,China Three Gorges University,Hubei Yichang 443001,China;Clinical Medical Research Center,Yichang Sports Injury and Repair,Hubei Yichang 443001,China;Third-grade Pharmacological Laboratory for Traditional Chinese Medicine Approved by State Administration of Traditional Chinese Medicine,China Three Gorges University,Hubei Yichang 443001,China)
机构地区:[1]三峡大学附属仁和医院骨科,湖北宜昌443001 [2]三峡大学运动医学研究所,湖北宜昌443001 [3]宜昌市运动损伤与修复临床医学研究中心,湖北宜昌443001 [4]三峡大学国家中医药管理局中药药理(肿瘤)科研三级实验室,湖北宜昌443001
出 处:《中国药房》2023年第7期892-896,共5页China Pharmacy
基 金:湖北省科技创新专项立项项目(No.2021CFB414);湖北省卫生健康委员会中医药科研项目(No.ZY2021M074)。
摘 要:类风湿关节炎(RA)是一种慢性系统性自身免疫性疾病,炎症细胞浸润、血管翳形成、关节软骨破坏和骨基质破坏是其主要特征,因此,改善关节软骨破坏对RA的治疗具有重要影响。中药因具有多成分、多靶点、高活性、少副作用等特点,在改善RA软骨破坏方面具有较好的应用效果。笔者查阅相关文献,对中药及其活性成分改善RA软骨破坏的作用机制进行归纳总结:中药及其活性成分可通过调控炎症因子,磷脂酰肌醇3-激酶/蛋白激酶B、Wnt/β-catenin、核因子κB、促分裂原活化的蛋白激酶、JAK2激酶/信号转导和转录激活因子3/血管内皮生长因子等信号通路,微小RNA以及成纤维样滑膜细胞来改善RA软骨破坏。Rheumatoid arthritis(RA)is a systemic chronic auto-inflammatory disease,characterized by infiltration of inflammatory cells,pannus formation,articular cartilage destruction,and bone matrix destruction.Therefore,improving articular cartilage destruction has an important impact on the treatment of RA.Chinese medicine has a good application effect in improving cartilage destruction of RA due to its characteristics of multiple components,multiple targets,high activity and low side effects.Based on this,the author reviewed relevant literature to summarize the relevant research and mechanism of Chinese medicine and its active components in improving RA cartilage destruction.The results showed that Chinese medicine and its active components can improve RA cartilage destruction by regulating inflammatory factors,phosphatidylinositol 3-kinase/protein kinase B,Wnt/β-catenin,nuclear factor-κB,mitogen-activated protein kinase,Janus kinase 2/signal transduction and activator of transcription 3/vascular endothelial growth factor,microRNAs,fibroblastic synovial cells.
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